The Brain: Our Food-Traffic Controller By KATHLEEN A. PAGE and ROBERT S. SHERWIN IMAGINE that, instead of this article, you were staring at a plate of freshly baked chocolate chip cookies. The mere sight and smell of them would likely make your mouth water. The first bite would be enough to wake up brain areas that control reward, pleasure and emotion — and perhaps trigger memories of when you tasted cookies like these as a child. That first bite would also stimulate hormones signaling your brain that fuel was available. The brain would integrate these diverse messages with information from your surroundings and make a decision as to what to do next: keep on chewing, gobble down the cookie and grab another, or walk away. Studying the complex brain response to such sweet temptations has offered clues as to how we might one day control a profound health problem in the country: the obesity epidemic. The answer may partly lie in a primitive brain region called the hypothalamus. The hypothalamus, which monitors the body’s available energy supply, is at the center of the brain’s snack-food signal processing. It keeps track of how much long-term energy is stored in fat by detecting levels of the fat-derived hormone leptin — and it also monitors the body’s levels of blood glucose, minute-to-minute, along with other metabolic fuels and hormones that influence satiety. When you eat a cookie, the hypothalamus sends out signals that make you less hungry. Conversely, when food is restricted, the hypothalamus sends signals that increase your desire to ingest high-calorie foods. The hypothalamus is also wired to other brain areas that control taste, reward, memory, emotion and higher-level decision making. These brain regions form an integrated circuit that was designed to control the drive to eat. © 2013 The New York Times Company

Keyword: Obesity; Attention
Link ID: 18087 - Posted: 04.28.2013

By VATSAL G. THAKKAR IN the spring of 2010, a new patient came to see me to find out if he had attention-deficit hyperactivity disorder. He had all the classic symptoms: procrastination, forgetfulness, a propensity to lose things and, of course, the inability to pay attention consistently. But one thing was unusual. His symptoms had started only two years earlier, when he was 31. Though I treat a lot of adults for attention-deficit hyperactivity disorder, the presentation of this case was a violation of an important diagnostic criterion: symptoms must date back to childhood. It turned out he first started having these problems the month he began his most recent job, one that required him to rise at 5 a.m., despite the fact that he was a night owl. The patient didn’t have A.D.H.D., I realized, but a chronic sleep deficit. I suggested some techniques to help him fall asleep at night, like relaxing for 90 minutes before getting in bed at 10 p.m. If necessary, he could take a small amount of melatonin. When he returned to see me two weeks later, his symptoms were almost gone. I suggested he call if they recurred. I never heard from him again. Many theories are thrown around to explain the rise in the diagnosis and treatment of A.D.H.D. in children and adults. According to the Centers for Disease Control and Prevention, 11 percent of school-age children have now received a diagnosis of the condition. I don’t doubt that many people do, in fact, have A.D.H.D.; I regularly diagnose and treat it in adults. But what if a substantial proportion of cases are really sleep disorders in disguise? © 2013 The New York Times Company

Keyword: Sleep; ADHD
Link ID: 18086 - Posted: 04.28.2013

By LINDA LOGAN The last time I saw my old self, I was 27 years old and living in Boston. I was doing well in graduate school, had a tight circle of friends and was a prolific creative writer. Married to my high-school sweetheart, I had just had my first child. Back then, my best times were twirling my baby girl under the gloaming sky on a Florida beach and flopping on the bed with my husband — feet propped against the wall — and talking. The future seemed wide open. I don’t think there is a particular point at which I can say I became depressed. My illness was insidious, gradual and inexorable. I had a preview of depression in high school, when I spent a couple of years wearing all black, rimming my eyes in kohl and sliding against the walls in the hallways, hoping that no one would notice me. But back then I didn’t think it was a very serious problem. The hormonal chaos of having three children in five years, the pressure of working on a Ph.D. dissertation and a genetic predisposition for a mood disorder took me to a place of darkness I hadn’t experienced before. Of course, I didn’t recognize that right away. Denial is a gauze; willful denial, an opiate. Everyone seemed in league with my delusion. I was just overwhelmed, my family would say. I should get more help with the kids, put off my Ph.D. When I told other young mothers about my bone-wearying fatigue, they rolled their eyes knowingly and mumbled, “Right.” But what they didn’t realize was that I could scarcely push the stroller to the park, barely summon the breath to ask the store clerk, “Where are the Pampers?” I went from doctor to doctor, looking for the cause. Lab tests for anemia, low blood sugar and hypothyroidism were all negative. © 2013 The New York Times Company

Keyword: Schizophrenia
Link ID: 18085 - Posted: 04.28.2013

By Russell Foster "Making teens start school in the morning is ‘cruel,’ brain doctor claims." So declared a British newspaper headline in 2007 after a talk I gave at an academic conference. One disbelieving reader responded: "This man sounds brain-dead." That was a typical reaction to work I was reporting at the time on teenage sleep patterns and their effect on performance at school. Six years on, there is growing acceptance that the structure of the academic day needs to take account of adolescent sleep patterns. The latest school to adopt a later start time is the UCL Academy in London; others are considering following suit. So what are the facts about teenage slumber, and how should society adjust to these needs? The biology of human sleep timing, like that of other mammals, changes as we age. This has been shown in many studies. As puberty begins, bedtimes and waking times get later. This trend continues until 19.5 years in women and 21 in men. Then it reverses. At 55 we wake at about the time we woke prior to puberty. On average this is two hours earlier than adolescents. This means that for a teenager, a 7 a.m. alarm call is the equivalent of a 5 a.m. start for people in their 50s. Precisely why this is so is unclear, but the shifts correlate with hormonal changes at puberty and the decline in those hormones as we age. However, biology is only part of the problem. Additional factors include a more relaxed attitude to bedtimes by parents, a general disregard for the importance of sleep, and access to TVs, DVDs, PCs, gaming devices, cellphones, and so on, all of which promote alertness and eat into time available for sleep. © 2013 The Slate Group, LLC.

Keyword: Sleep; Development of the Brain
Link ID: 18084 - Posted: 04.27.2013

By David Levine Sleep deprivation is a quick and efficient way to treat depression. It works 60 to 70 percent of the time—far better than existing drugs—but the mood boost usually lasts only until the patient falls asleep. As an ongoing treatment, sleep deprivation is impractical, but researchers have been studying the phenomenon in an effort to uncover the cellular mechanisms behind depression and remission. Now a team at Tufts University has pinpointed glia as the key players. The researchers previously found that astrocytes, a star-shaped type of glial cell, regulate the brain chemicals involved in sleepiness. During our waking hours, astrocytes continuously release the neurotransmitter adenosine, which builds up in the brain and causes “sleep pressure,” the feeling of sleepiness and its related memory and attention impairments. The neurotransmitter causes this pressure by binding to adenosine receptors on the outside of neurons like a key fitting into a lock. As more adenosine builds up, more receptors are triggered, and the urge to sleep gets stronger. In the new study, published online January 15 in the journal Translational Psychiatry, the scientists investigated whether this process is responsible for the antidepressant effects of sleep deprivation. Mice with depressivelike symptoms were administered three doses of a compound that triggers adenosine receptors, thus mimicking sleep deprivation. Although the mice continued to sleep normally, after 12 hours they showed a rapid improvement in mood and behavior, which lasted for 48 hours. © 2013 Scientific American

Keyword: Depression; Sleep
Link ID: 18083 - Posted: 04.27.2013

by Emily Underwood In the cartoon series named after them, Pinky and the Brain, two laboratory mice genetically enhanced to increase their intelligence plot to take over the world—and fail each time. Perhaps their creators hadn't tweaked the correct gene. Researchers have now found a genetic mutation that causes mammalian neural tissue to expand and fold. The discovery may help explain why humans evolved more elaborate brains than mice, and it could suggest ways to treat disorders such as autism and epilepsy that arise from abnormal neural development. In mice and humans alike, the cerebral cortex—the outermost layer of brain tissue associated with high-level functions such as memory and decision-making—starts out as a spherical sheet of tissue made up of only neural stem cells. As these stem cells divide, the cortex increases its surface area, expanding like an inflating balloon, says neuroscientist Victor Borrell of the Institute of Neurosciences of Alicante in Spain. Unlike the small, smooth mouse brain, however, the uppermost layers of tissue in the human brain cram millions of neurons into specialized folds and furrows responsible for complex tasks such as language and thought. Because the human cerebral cortex is generally considered "special," some scientists have hypothesized that the genes that govern its development of cortical folds and furrows are also unique to humans, Borrell says. In studies of neural development in mice, Stahl found that TRNP1 produces a protein that determines whether neural stem cells self-replicate, leading to a balloonlike expansion of cortical surface area, or whether they differentiate into a plethora of intermediate stem cell types and neurons, thickening the cortex and forming more complex brain structures. Based on that discovery, the team hypothesized that varying levels of the gene's expression in mice and humans might account for the varying levels of cortical thickness and different shapes between the two species. © 2010 American Association for the Advancement of Science

Keyword: Development of the Brain; Genes & Behavior
Link ID: 18082 - Posted: 04.27.2013

by Dr. Claire McCarthy April is Autism Awareness Month--and if there's anything that we need when it comes to autism, it's awareness. We need people to be aware of this condition that affects a staggering 1 in 50 children, so that we can understand what causes it, and find ways to prevent it. And we need people to be aware of the signs of autism--because getting help early can make a real difference. Many children aren't diagnosed with autism until they get to preschool, or sometimes even later--and that means important time is lost. The signs of autism can be present in toddlers--and when we find it then, we can get help to those children and their families right away. The trick is in asking the right questions--and acting on the answers. In the practice where I work, as in many other practices, we ask parents to fill out questionnaires about the behavior and development of their children. At the 18 month and 24 month visits, we ask parents to fill out one called the MCHAT (Modified Checklist for Autism in Toddlers)--that's the tool we've chosen to help us look for autism. It's a list of questions that parents answer yes or no to, questions about how their child acts, plays and interacts with other people. While all the questions on the MCHAT are important, there are six that are most important: Does your child take an interest in other children? Does your child ever use his finger to point at or ask for something? Does your child ever bring objects over to you to show you something? Does your child imitate you? Does your child respond to his name when you call? If you point at a toy across the room, does your child look at it? © 2013 NY Times Co.

Keyword: Autism
Link ID: 18081 - Posted: 04.27.2013

By Karen Rowan and MyHealthNewsDaily Children at an increased risk of autism may have abnormal structures in the placenta that can be detected at birth, a new study finds. The findings suggest behavioral interventions aimed at social and motor skill development in these children could be started right away, the researchers said. Studies have shown that such interventions are more effective in children with autism when they are started earlier. It's much too early to say that an examination of the placenta could be used as a definitive test for autism at birth, said study researcher Dr. Harvey Kliman, director of Reproductive and Placental Research at the Yale University School of Medicine. Autism spectrum disorders are typically diagnosed when children are ages 3 or 4, or even older. However, if these structures were found upon a child's birth and interventions were started, the child might benefit greatly if they did turn out to have autism, while there would be little downside if a child turned out not to have autism -- it's unlikely they would be harmed by the effort, Kliman said. In the study, Kliman and his colleagues collected samples of placenta tissue from 117 children born to families who already had a child with autism, and compared them with placentas from 100 babies born into families in which no older children had autism. The researchers, who didn't know which placentas had come from each group of children, examined samples of the placentas under microscopes. © 2013 Scientific American

Keyword: Autism; Development of the Brain
Link ID: 18080 - Posted: 04.27.2013

Karen Ravn Birds of a feather may flock together, but do birds that flock together develop distinct cultures? Two studies published today in Science1, 2 find strong evidence that, at the very least, monkeys that troop together and whales that pod together do just that. And they manage it in the same way that humans do: by copying and learning from each other. A team led by Erica van de Waal, a primate psychologist at the University of St Andrews, UK, created two distinct cultures — 'blue' and 'pink' — among groups of wild vervet monkeys (Chlorocebus aethiops) in South Africa1. The researchers trained two sets of monkeys to eat maize (corn) dyed one of those two colours but eschew maize dyed the other colour. The scientists then waited to see how the groups behaved when newcomers — babies and migrating males — arrived. Both sets of newcomers seemed to follow social cues when selecting their snacks. Baby monkeys ate the same colour maize as their mothers. Seven of the ten males that migrated from one colour culture to another adopted the local colour preference the first time that they ate any maize. The trend was even stronger when they first fed with no higher-ranking monkey around, with nine of the ten males choosing the locally preferred variety. The only immigrant to buck this trend was a monkey who assumed the top rank in his new group as soon as he got there — and he may not have given a fig what anyone else ate. “The take-home message is that social learning — learning from others rather than through individual trial and error — is a more potent force in shaping wild animals’ behaviour than has been recognized so far,” says Andrew Whiten, an evolutionary and developmental psychologist at St Andrews and co-author of the paper. © 2013 Nature Publishing Group

Keyword: Learning & Memory; Evolution
Link ID: 18079 - Posted: 04.27.2013

Posted by Christy Ullrich Elephants may use a variety of subtle movements and gestures to communicate with one another, according to researchers who have studied the big mammals in the wild for decades. To the casual human observer, a curl of the trunk, a step backward, or a fold of the ear may not have meaning. But to an elephant—and scientists like Joyce Poole—these are signals that convey vital information to individual elephants and the overall herd. Biologist and conservationist Joyce Poole and her husband, Petter Granli, both of whom direct ElephantVoices, a charity they founded to research and advocate for conservation of elephants in various sanctuaries in Africa, have developed an online database decoding hundreds of distinct elephant signals and gestures. The postures and movements underscore the sophistication of elephant communication, they say. Poole and Granli have also deciphered the meaning of acoustic communication in elephants, interpreting the different rumbling, roaring, screaming, trumpeting, and other idiosyncratic sounds that elephants make in concert with postures such as the positioning and flapping of their ears. Poole has studied elephants in Africa for more than 37 years, but only began developing the online gestures database in the past decade. Some of her research and conservation work has been funded by the National Geographic Society. “I noticed that when I would take out guests visiting Amboseli [National Park in Kenya] and was narrating the elephants’ behavior, I got to the point where 90 percent of the time, I could predict what the elephant was about to do,” Poole said in an interview. “If they stood a certain way, they were afraid and were about to retreat, or [in another way] they were angry and were about to move toward and threaten another.” © 1996-2012 National Geographic Society.

Keyword: Language; Evolution
Link ID: 18078 - Posted: 04.27.2013

by Helen Thomson "I feel like I have been dropped into my body. I know this is my voice and these are my memories, but they don't feel like they belong to me." It happened out of the blue. Louise Airey was 8 years old, off sick from school, when suddenly she felt like she had been dropped into her own body. "It's just so difficult to verbalise what this feels like," she says. "All of a sudden you're hyper aware, and everything else in the world seems unreal, like a movie." She panicked, but told no one. The feeling soon passed but returned several times until, at the age of 19, a migraine triggered a sensation of being disconnected from the world that was to last 18 months. When she was in her 30s she was diagnosed with depersonalisation disorder – an altered sense of self with all-encompassing feelings of not occupying your own body, and detachment from your thoughts and actions. It has come and gone throughout her life, but since a traumatic pregnancy 20 months ago, these feelings have remained constant. "Other people seem like robots," Airey says. "It's like I'm watching a film, like I'm on my own in the centre of everything and nothing else is real. I'll be speaking to my children and I'll catch my voice talking and it seems really alien and foreign. It makes you feel very separated and lonely from everything, like you're the only person that is real." Depersonalisation disorder is not as rare as you might think, says Anthony David at King's College London and the Maudsley Hospital: it may affect almost 1 per cent of the British population (Social Psychiatry and Psychiatric Epidemiology, DOI: 10.1007/s00127-010-0327-7). We've all probably experienced mild versions of it at some point, in the unreal, spaced-out feeling you might get while severely jet-lagged or hung-over, for example. © Copyright Reed Business Information Ltd.

Keyword: Attention
Link ID: 18077 - Posted: 04.27.2013

Sunanda Creagh, The Conversation Testosterone may trigger a brain chemical process linked to schizophrenia but the same sex hormone can also improve cognitive thinking skills in men with the disorder, two new studies show. Scientists have long suspected testosterone plays an important role in schizophrenia, which affects more men than women. Men are also more likely to develop psychosis in adolescence, previous research has shown. A new study on lab rodents by researchers from Neuroscience Research Australia analysed the impact increased testosterone had on levels of dopamine, a brain chemical linked to psychotic symptoms of schizophrenia. The researchers found that testosterone boosted dopamine sensitivity in adolescent male rodents. “From these rodent studies, we hypothesise that adolescent increases in circulating testosterone may be a driver of increased dopamine activity in the brains of individuals susceptible to psychosis and schizophrenia,” said senior Neuroscience Research Australia researcher and author of the study, Dr Tertia Purves-Tyson, who is presenting her work at the International Congress on Schizophrenia Research in Florida. Dr Philip Mitchell, Scientia Professor and Head of the School of Psychiatry at the University of NSW, said the research was very interesting. © 2013 ScienceAlert Pty Ltd.

Keyword: Schizophrenia; Hormones & Behavior
Link ID: 18076 - Posted: 04.27.2013

by Sara Reardon An electronic patch can analyse complex brainwaves and listen in on a fetus’s heart MIND reading can be as simple as slapping a sticker on your forehead. An "electronic tattoo" containing flexible electronic circuits can now record some complex brain activity as accurately as an EEG. The tattoo could also provide a cheap way to monitor a developing fetus. The first electronic tattoo appeared in 2011, when Todd Coleman at the University of California, San Diego, and colleagues designed a transparent patch containing electronic circuits as thin as a human hairMovie Camera. Applied to skin like a temporary tattoo, these could be used to monitor electrophysiological signals associated with the heart and muscles, as well as rudimentary brain activity. To improve its usefulness, Coleman's group has now optimised the placement of the electrodes to pick up more complex brainwaves. They have demonstrated this by monitoring so-called P300 signals in the forebrain. These appear when you pay attention to a stimulus. The team showed volunteers a series of images and asked them to keep track of how many times a certain object appeared. Whenever volunteers noticed the object, the tattoo registered a blip in the P300 signal. The tattoo was as good as conventional EEG at telling whether a person was looking at the target image or another stimulus, the team told a recent Cognitive Neuroscience Society meeting in San Francisco. © Copyright Reed Business Information Ltd.

Keyword: Brain imaging; Robotics
Link ID: 18075 - Posted: 04.27.2013

Published by scicurious under Behavioral Neuro It's late. I've got a lot on my plate. A lot to do. And most of us do. So here I am, burning the midnight oil along with many of my neighbors. I usually count myself lucky to get 7 hours a night, and I AM lucky. For many parents or other caregivers, for example, 7 hours is unheard-of luxury. Is it just me? Probably not. Most of us don't get enough sleep, and those who don't sleep? Snack. But why? And what does this mean for issues like obesity? We know that there has been an increase in obesity in this country. And many people are asking why. There are probably lots of reasons involved: too much sugar, too little exercise, genetics, too much fat. But what about sleep? It turns out that getting less sleep is a risk factor for obesity, but...how are sleep and weight gain related? It turns out that sleep, or lack thereof, can have a lot of influence on how much we need to eat and how much we feel like eating. For example, sleep deprivation changes hunger hormone levels, which can change food intake, and some scientists hypothesize that decreased sleep can change energy expenditure as well. But in order to understand just how lack of sleep influences weight gain, well you need to sleep deprive some people. The authors took 8 men and 8 women who reported getting an average of 8 hours of sleep per night into an inpatient facility. They were taken off caffeine one week before the study and were told to stick to 9 hours of sleep opportunity (stay in bed 9 hours) per night for the first week. They also were put on a diet that was calibrated exactly to maintain their current weight. Copyright © 2013

Keyword: Sleep; Obesity
Link ID: 18074 - Posted: 04.25.2013

David Adam David Kupfer is a modern-day heretic. A psychiatrist at the University of Pittsburgh in Pennsylvania, Kupfer, has spent the past six years directing the revision of a book commonly referred to as the bible of the psychiatric field. The work will reach a climax next month when the American Psychiatric Association (APA) unveils the fifth incarnation of the book, called the Diagnostic and Statistical Manual of Mental Disorders (DSM), which provides checklists of symptoms that psychiatrists around the world use to diagnose their patients. The DSM is so influential that just about the only suggestion of Kupfer's that did not meet with howls of protest during the revision process was to change its name from DSM-V to DSM-5. Although the title and wording of the manual are now settled, the debate that overshadowed the revision is not. The stark fact is that no one has yet agreed on how best to define and diagnose mental illnesses. DSM-5, like the two preceding editions, will place disorders in discrete categories such as major-depressive disorder, bipolar disorder, schizophrenia and obsessive–compulsive disorder (OCD). These categories, which have guided psychiatry since the early 1980s, are based largely on decades-old theory and subjective symptoms. The problem is that biologists have been unable to find any genetic or neuroscientific evidence to support the breakdown of complex mental disorders into separate categories. Many psychiatrists, meanwhile, already think outside the category boxes, because they see so many patients whose symptoms do not fit neatly into them. Kupfer and others wanted the latest DSM to move away from the category approach and towards one called 'dimensionality', in which mental illnesses overlap. According to this view, the disorders are the product of shared risk factors that lead to abnormalities in intersecting drives such as motivation and reward anticipation, which can be measured (hence 'dimension') and used to place people on one of several spectra. But the attempt to introduce this approach foundered, as other psychiatrists and psychologists protested that it was premature. © 2013 Nature Publishing Group

Keyword: Schizophrenia; Depression
Link ID: 18073 - Posted: 04.25.2013

By Lucy Wallis BBC News Abby and Brittany Hensel are conjoined twins determined to live the normal, active life of outgoing 20-somethings anywhere. They have been to university, they travel, they have jobs. But how easy is it for two people to inhabit one body? Like most 23-year-olds Abby and Brittany Hensel love spending time with their friends, going on holiday, driving, playing sport such as volleyball and living life to the full. The identical, conjoined twins from Minnesota, in the United States, have graduated from Bethel University and are setting out on their career as primary school teachers with an emphasis on maths. Although they have two teaching licences, there is one practical difference when it comes to the finances. "Obviously right away we understand that we are going to get one salary because we're doing the job of one person," says Abby. "As maybe experience comes in we'd like to negotiate a little bit, considering we have two degrees and because we are able to give two different perspectives or teach in two different ways." "One can be teaching and one can be monitoring and answering questions," says Brittany. "So in that sense we can do more than one person." Their friend Cari Jo Hohncke has always admired the sisters' teamwork. "They are two different girls, but yet they are able to work together to do the basic functions that I do every day that I take for granted," says Hohncke. BBC © 2013

Keyword: Laterality
Link ID: 18072 - Posted: 04.25.2013

By Meghan Holohan Need to remember some important facts for that big presentation at work? Clench your right hand while preparing to remember. When giving that talk, ball up your left hand and you’ll call to mind those details, no problem. That’s the finding from a new study authored by Ruth Propper, an associate professor and director of the cerebral lateralization laboratory at Montclair State University. Propper has long been intrigued by how body movements impact how the brain works. While most people realize that the brain influences the body (the brain tells your arm there is an itch, and you feel it), less is understood about how the body sways the brain. Past research suggests that clenching our hands can evoke emotions. When people ball up their right hands, for example, the left sides of their brains become more active, causing what’s known as “approach emotions,” feelings such as happiness or excitement. By squeezing the left hand, people engage the right side of the brain, which controls “withdrawal emotions” such as introversion, fear, or anxiety. (It probably seems like these might be less useful, but they come in handy in dangerous situations.) Propper theorized that if clenching hands impacted feelings, these gestures might influence the brain in other ways. © 2013 NBCNews.com

Keyword: Learning & Memory; Laterality
Link ID: 18071 - Posted: 04.25.2013

By KATIE THOMAS With the diagnosis of autism on the rise and drug companies facing major setbacks in developing successful treatments, the University of California, Los Angeles will lead a $9 million effort financed by the National Institute of Mental Health to find effective drugs, officials said Wednesday. Under a contract with the institute, U.C.L.A. will form a network of researchers at other academic centers that will try to identify promising new and older drug compounds quickly, and conduct early tests to see if they merit additional investment. The program, part of the “Fast Fail” initiative at the institute, aims to determine within weeks whether a drug works, rather than the years it traditionally takes to evaluate a new drug. “The whole idea is just getting much better in these early phases at identifying drugs that are going to be efficacious and safe, and thereby greatly speeding the development of effective new therapies and reducing the overall cost,” said Dr. James McCracken, who is leading the effort at U.C.L.A. as director of the division of child and adolescent psychiatry at the Semel Institute for Neuroscience and Human Behavior. The number of diagnosed cases of autism, Asperger’s syndrome and related disorders in children has been growing in recent years, largely because of increased awareness. A recent report by the Centers for Disease Control and Prevention and the Health Resources and Services Administration concluded that one in 50 children aged 6 to 17 had been found to have autism or a related disorder, a 72 percent increase since 2007. Although more cases are being diagnosed, no drugs are approved to treat the core symptoms of the disorders, which are characterized by delays in developing effective communication and social skills. Other drugs often prescribed to people with the disorders treat difficult behaviors like aggressiveness, hyperactivity and irritability. © 2013 The New York Times Company

Keyword: Autism
Link ID: 18070 - Posted: 04.25.2013

By PAM BELLUCK After most pregnancies, the placenta is thrown out, having done its job of nourishing and supporting the developing baby. But a new study raises the possibility that analyzing the placenta after birth may provide clues to a child’s risk for developing autism. The study, which analyzed placentas from 217 births, found that in families at high genetic risk for having an autistic child, placentas were significantly more likely to have abnormal folds and creases. “It’s quite stark,” said Dr. Cheryl K. Walker, an obstetrician-gynecologist at the Mind Institute at the University of California, Davis, and a co-author of the study, published in the journal Biological Psychiatry. “Placentas from babies at risk for autism, clearly there’s something quite different about them.” Researchers will not know until at least next year how many of the children, who are between 2 and 5, whose placentas were studied will be found to have autism. Experts said, however, that if researchers find that children with autism had more placental folds, called trophoblast inclusions, visible after birth, the condition could become an early indicator or biomarker for babies at high risk for the disorder. “It would be really exciting to have a real biomarker and especially one that you can get at birth,” said Dr. Tara Wenger, a researcher at the Center for Autism Research at Children’s Hospital of Philadelphia, who was not involved in the study. © 2013 The New York Times Company

Keyword: Autism; Development of the Brain
Link ID: 18069 - Posted: 04.25.2013

By Stephen L. Macknik Why, oh why, would I order a plastic fork, costing $89 (on-sale), 5 months before its scheduled release? Because it promises to help me control my eating speed, which, I am now convinced, is indeed critical to controlling obesity and diabetes. The fork is essentially a Bluetooth device that communicates to your smartphone and counts how many bites you take each meal. More importantly, I believe it counts the amount of time between each bite and if you go too fast, it vibrates. [Insert vibrator to mouth joke here. Yes, I'm blonde.] The reason I think it will help me goes back to my gastric bypass two months ago. Before and after the surgery, patients of Dr. Robin Blackmore at the Scottsdale Healthcare Bariatric Surgery Unit must take a series of courses aimed at preparing patients for life after surgery. One of the main lessons is that patients must now eat each meal over a 20 minute period. No more, no less. As you might surmise, for patients like me, “no more” is ready to achieve, but “no less” than 20 minutes is surprisingly difficult. And they are well aware of how hard it is, demanding that you practice ahead of time. I don’t know about my fellow patients, but I didn’t practice at all and have paid the price numerous times since my surgery for eating too fast: let’s just say it sometimes leads to a temporary obstruction and leave it at that. Because the details are unbelievably disgusting. © 2013 Scientific American,

Keyword: Obesity
Link ID: 18068 - Posted: 04.24.2013